Author + information
- Received May 11, 1987
- Revision received September 15, 1987
- Accepted September 28, 1987
- Published online February 1, 1988.
- Douglas Triffon, MD,
- Bertron M. Groves, MD, FACC,
- John T. Reeves, MD, FACC and
- Roy V. Ditchey, MD, FACC∗
- ↵∗Address for correspondence: Roy V. Ditchey, MD, Cardiology Unit, Medical Center Hospital of Vermont, Burlington, Vermont 05401.
Previous studies have suggested that right ventricular systolic pressure can be predicted from noninvasive estimates of the interval between pulmonary valve closure and tricuspid valve opening. To determine the basis for this relation, phonocardiograms and high fidelity right atrial and ventricular pressures were recorded in 29 patients with a right ventricular systolic pressure ranging from 20 to 149 mm Hg. In 22 patients with normal right atrial pressure (⩽ 8 mm Hg), both the time interval and the magnitude of pressure decrease from pulmonary valve closure to tricuspid valve opening were linearly related to systolic pressure (r = 0.89 and 0.96, respectively). Early pulmonary valve closure (decreased “hang-out” time) contributed to the greater magnitude of isovolumic pressure decrease at high systolic pressures, but correction for hang-out time did not eliminate the relation between systolic pressure and the pulmonary valve closure-tricuspid valve opening interval (n = 10).
When patients with documented right coronary artery disease were excluded, the time constant for isovolumic pressure decrease also increased as a function of systolic pressure (r = 0.67, p < 0.01, n = 24), suggesting impaired relaxation at high systolic pressures. However, the mean rate of pressure decrease (mean negative dP/dt) still was greater in patients with a high pressure because of the exponential nature of the isovolumic pressure-time relation. The pulmonary valve closure-tricuspid valve opening interval accurately predicted normal systolic pressure in patients with right coronary artery disease despite markedly prolonged time constants, but was inappropriately short for the level of systolic pressure in patients with an elevated mean right atrial pressure because early opening of the tricuspid valve decreased the magnitude of isovolumic pressure fall.
These findings indicate that 1) the magnitude of isovolumic pressure fall is the major determinant of the pulmonary valve closure-tricuspid valve opening interval, 2) pulmonary hypertension prolongs the interval by increasing both the magnitude and the time constant for pressure fall, and 3) the determinants of this interval can be altered by factors other than systolic pressure.
☆ This study was supported in part by grants from the National Heart, Lung, and Blood Institute (HL-14985) and the Clinical Research Center Branch (RR-00051) of the National Institutes of Health, Bethesda, Maryland.
- Received May 11, 1987.
- Revision received September 15, 1987.
- Accepted September 28, 1987.